A decrease in circulating calcium due to vitamin D deficiency, inefficient vitamin D metabolism, and/or calcium deficiency triggers the release of PTH, which stimulates renal expression of 1α-hydroxylase to increase the synthesis of 1,25-(OH)2D. The main functions of this active form are the enhancement of intestinal calcium absorption, the reduction of urinary excretion of calcium, and the increase in the formation of osteoclasts leading to bone resorption, finally releasing calcium into the blood and restoring calcium levels [7]. This evidence concerns the gene PTH and vitamin D deficiency.